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Allergic eosinophil-rich inflammation develops in lungs and airways of B cell-deficient mice.

Korsgren M, Erjefält JS, Korsgren O, Sundler F, Persson CG - J. Exp. Med. (1997)

Bottom Line: Immunoglobulins (Ig), particularly IgE, are believed to be crucially involved in the pathogenesis of asthma and, equally, in allergic models of the disease.The eosinophilia extended to the regional lymph nodes.TEM confirmed the subepithelial and perivascular localization of eosinophils.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology and Neuroscience, Lund University Hospital, Sweden.

ABSTRACT
Immunoglobulins (Ig), particularly IgE, are believed to be crucially involved in the pathogenesis of asthma and, equally, in allergic models of the disease. To validate this paradigm we examined homozygous mutant C57BL/6 mice, which are B cell deficient, lacking all Ig. Mice were immunized intraperitoneally with 10 micrograms ovalbumin (OVA) plus alum, followed by daily (day 14-20) 30 min exposures to OVA aerosol (OVA/OVA group). Three control groups were run: OVA intraperitoneally plus saline (SAL) aerosol (OVA/SAL group); saline intraperitoneally plus saline aerosol; saline intraperitoneally plus OVA aerosol (n = 6-7). Lung and large airway tissues obtained 24 h after the last OVA or SAL exposure were examined by light microscopy and transmission electron microscopy (TEM). The Ig-deficient mice receiving OVA/ OVA treatment had swollen and discolored lungs and exhibited marked eosinophilia both in large airway subepithelial tissue (49.2 +/- 12.0 cells/mm basement membrane [BM] versus OVA/ SAL control 1.2 +/- 0.3 cells/mm BM; P < 0.001), and perivascularly and peribronchially in the lung (49.3 +/- 9.0 cells/unit area versus OVA/SAL control 2.6 +/- 0.6 cells/unit area; P < 0.001). The eosinophilia extended to the regional lymph nodes. TEM confirmed the subepithelial and perivascular localization of eosinophils. Mucus cells in large airway epithelium increased from 1.5 +/- 0.8 (OVA/SAL mice) to 39.5 +/- 5.7 cells/mm BM in OVA/OVA treated mice (P < 0.001). OVA/SAL mice never differed from the other control groups. Corresponding experiments in wild-type mice (n = 6-7 in each group) showed qualitatively similar but less pronounced eosinophil and mucus cell changes. Macrophages and CD4+ T cells increased in lungs of all OVA/OVA-treated mice. Mast cell number did not differ but degranulation was detected only in OVA/OVA-treated wild-type mice. Immunization to OVA followed by OVA challenges thus cause eosinophil-rich inflammation in airways and lungs of mice without involvement of B cells and Ig.

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Lung histology.  Eosinophils are visualized by histochemical demonstration of cyanide-resistant eosinophil peroxidase activity. Multifocal perivascular  and peribronchial eosinophilic  distribution in the lung tissue is  seen in immunized and OVAchallenged Ig-deficient (a) and  wild-type (b) mice. No eosinophilic infiltrates were observed in  lung tissue from control mice of  either the Ig-deficient (c) or the  wild-type (d) mice. B, bronchus;  V, blood vessel. Bar, 60 μm.
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Figure 1: Lung histology. Eosinophils are visualized by histochemical demonstration of cyanide-resistant eosinophil peroxidase activity. Multifocal perivascular and peribronchial eosinophilic distribution in the lung tissue is seen in immunized and OVAchallenged Ig-deficient (a) and wild-type (b) mice. No eosinophilic infiltrates were observed in lung tissue from control mice of either the Ig-deficient (c) or the wild-type (d) mice. B, bronchus; V, blood vessel. Bar, 60 μm.

Mentions: On gross examination during the tissue dissection, the lungs of OVA/OVA-treated animals appeared swollen and discoloured. These animals, of both the Ig deficient and wild type, showed a multifocal perivascular and peribronchial eosinophilic distribution in the lung tissue (Fig. 1, a–b) and marked eosinophilic infiltrates occurred in the large airway tissue and in the tracheobronchial lymph nodes (Table 1). There was a particularly dense infiltration of eosinophils in the tracheobronchial lymph nodes of Igdeficient mice (Fig. 2). Eosinophilic infiltrates were not observed in lung or large airway tissue from control mice of either the wild-type or the Ig-deficient type (Fig. 1, c–d; Table 1).


Allergic eosinophil-rich inflammation develops in lungs and airways of B cell-deficient mice.

Korsgren M, Erjefält JS, Korsgren O, Sundler F, Persson CG - J. Exp. Med. (1997)

Lung histology.  Eosinophils are visualized by histochemical demonstration of cyanide-resistant eosinophil peroxidase activity. Multifocal perivascular  and peribronchial eosinophilic  distribution in the lung tissue is  seen in immunized and OVAchallenged Ig-deficient (a) and  wild-type (b) mice. No eosinophilic infiltrates were observed in  lung tissue from control mice of  either the Ig-deficient (c) or the  wild-type (d) mice. B, bronchus;  V, blood vessel. Bar, 60 μm.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2196175&req=5

Figure 1: Lung histology. Eosinophils are visualized by histochemical demonstration of cyanide-resistant eosinophil peroxidase activity. Multifocal perivascular and peribronchial eosinophilic distribution in the lung tissue is seen in immunized and OVAchallenged Ig-deficient (a) and wild-type (b) mice. No eosinophilic infiltrates were observed in lung tissue from control mice of either the Ig-deficient (c) or the wild-type (d) mice. B, bronchus; V, blood vessel. Bar, 60 μm.
Mentions: On gross examination during the tissue dissection, the lungs of OVA/OVA-treated animals appeared swollen and discoloured. These animals, of both the Ig deficient and wild type, showed a multifocal perivascular and peribronchial eosinophilic distribution in the lung tissue (Fig. 1, a–b) and marked eosinophilic infiltrates occurred in the large airway tissue and in the tracheobronchial lymph nodes (Table 1). There was a particularly dense infiltration of eosinophils in the tracheobronchial lymph nodes of Igdeficient mice (Fig. 2). Eosinophilic infiltrates were not observed in lung or large airway tissue from control mice of either the wild-type or the Ig-deficient type (Fig. 1, c–d; Table 1).

Bottom Line: Immunoglobulins (Ig), particularly IgE, are believed to be crucially involved in the pathogenesis of asthma and, equally, in allergic models of the disease.The eosinophilia extended to the regional lymph nodes.TEM confirmed the subepithelial and perivascular localization of eosinophils.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology and Neuroscience, Lund University Hospital, Sweden.

ABSTRACT
Immunoglobulins (Ig), particularly IgE, are believed to be crucially involved in the pathogenesis of asthma and, equally, in allergic models of the disease. To validate this paradigm we examined homozygous mutant C57BL/6 mice, which are B cell deficient, lacking all Ig. Mice were immunized intraperitoneally with 10 micrograms ovalbumin (OVA) plus alum, followed by daily (day 14-20) 30 min exposures to OVA aerosol (OVA/OVA group). Three control groups were run: OVA intraperitoneally plus saline (SAL) aerosol (OVA/SAL group); saline intraperitoneally plus saline aerosol; saline intraperitoneally plus OVA aerosol (n = 6-7). Lung and large airway tissues obtained 24 h after the last OVA or SAL exposure were examined by light microscopy and transmission electron microscopy (TEM). The Ig-deficient mice receiving OVA/ OVA treatment had swollen and discolored lungs and exhibited marked eosinophilia both in large airway subepithelial tissue (49.2 +/- 12.0 cells/mm basement membrane [BM] versus OVA/ SAL control 1.2 +/- 0.3 cells/mm BM; P < 0.001), and perivascularly and peribronchially in the lung (49.3 +/- 9.0 cells/unit area versus OVA/SAL control 2.6 +/- 0.6 cells/unit area; P < 0.001). The eosinophilia extended to the regional lymph nodes. TEM confirmed the subepithelial and perivascular localization of eosinophils. Mucus cells in large airway epithelium increased from 1.5 +/- 0.8 (OVA/SAL mice) to 39.5 +/- 5.7 cells/mm BM in OVA/OVA treated mice (P < 0.001). OVA/SAL mice never differed from the other control groups. Corresponding experiments in wild-type mice (n = 6-7 in each group) showed qualitatively similar but less pronounced eosinophil and mucus cell changes. Macrophages and CD4+ T cells increased in lungs of all OVA/OVA-treated mice. Mast cell number did not differ but degranulation was detected only in OVA/OVA-treated wild-type mice. Immunization to OVA followed by OVA challenges thus cause eosinophil-rich inflammation in airways and lungs of mice without involvement of B cells and Ig.

Show MeSH
Related in: MedlinePlus